alexa Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions.


Atherosclerosis: Open Access

Author(s): Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM

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The current paradigm is based on the belief that type IV lesions, or “atheromas,” described by the AHA are stable because the fatty, necrotic core is contained by a smooth muscle cell–rich fibrous cap. Virchow’s analysis5 in 1858 pointed out that historically, the term “atheroma” refers to a dermal cyst (“Grützbalg”), a fatty mass encapsulated within a cap. Extending Virchow’s argument, the fibrous cap over the lipid mass of an atherosclerotic plaque is analogous to the capsule containing an abscess, and like an abscess, the plaque can be ruptured. Rupture of the fibrous cap exposes thrombogenic material, initiating platelet aggregation and coagulation in the infiltrating and overlying blood. These thrombotic changes result from activation of the clotting cascade by tissue factor, and further propagation of the thrombosis results from the interaction of platelets with the active thrombogenic matrix.6 Platelet activation and thrombin formation combined with the evulsion of thrombogenic plaque contents into the lumen then result in sudden occlusion.

This article was published in Arterioscler Thromb Vasc Biol and referenced in Atherosclerosis: Open Access

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